Metabolic rescue of a-synuclein-induced neurodegeneration through propionate supplementation and intestine-neuron signaling in C. elegans

Vitamin B12 depletion or propionate supplementation can reverse the transcriptomic aberration in the C. elegans model of PD with neuronal overexpression of alpha-synuclein A53T Overall design: C. elegans strains with pan-neuronal or dopaminergic neuron-specific overexpression of human alpha-synuclein A53T proteins were fed with either wild-type or B12-depleted cobS(-); cobA(-) K12 E. coli. The PD animals were also supplemented with either propionic acid or vitamin B12 to assess their effects on the transcriptome. Wild-type C. elegans carrying a transgene that expressed GFP in the dopaminergic neurons was used as a control strain. Animals were collected at L4 stage and subjected to whole-organism RNA sequencing. Ribosomal RNAs were depleted from the total RNA during the library construction.